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- 10.1101/gad.12.7.982
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Abstract
Downloaded from genesdev.cshlp.org on November 15, 2021 - Published by Cold Spring Harbor Laboratory Press CHOP is implicated in programmed cell death in response to impaired function of the endoplasmic reticulum 1 1 1 1 Helene Zinszner, Masahiko Kuroda, XiaoZhong Wang, Nikoleta Batchvarova, 2 3 2 1,4 Richard T. Lightfoot, Helen Remotti, James L. Stevens, and David Ron Skirball Institute of Biomolecular Medicine, the Departments of Medicine, Cell Biology, and the Kaplan Cancer Center, New York University (NYU) Medical Center, New York, New York 10016 USA; Adirondack Biomedical Research Facility, Lake Placid, New York 12946 USA; Department of Pathology, Cornell University Medical Center, New York, New York 10021 USA Cellular stress, particularly in response to toxic and metabolic insults that perturb function of the endoplasmic reticulum (ER stress), is a powerful inducer of the transcription factor CHOP. The role of CHOP in the response of cells to injury associated with ER stress was examined in a murine deficiency model obtained by homologous recombination at the chop gene. Compared with the wild type, mouse embryonic fibroblasts (MEFs) derived from chop −/− animals exhibited significantly less programmed cell death when challenged with agents that perturb ER function. A similar deficit in
Journal
Genes & Development – Unpaywall
Published: Apr 1, 1998